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Review Article| Volume 23, ISSUE 2, P277-284, May 2005

The Pathophysiology of Acute Pain

      The sensation of pain is a neural-biochemical phenomenon. When acute tissue damage occurs, neurochemical reactions at the site of injury activate the free nerve endings of special nerves called nociceptors. Nociceptors initiate an afferent nerve impulse that propagates through the peripheral nerve, enters the spinal cord, and synapses with higher order neurons. The impulse then traverses specific ascending spinal tracts, landing in cerebral centers for interpretation. Modulation of the afferent information can occur in many areas, including the periphery, spinal cord, midbrain, and cerebral cortex. Interpretation of the impulse yields a response signal, again traveling through specific descending spinal tracks and out through peripheral motor nerves. This process partially accounts for the delay in feeling a sensation of pain after experiencing an acute injury. Pain sensations can be categorized in many ways, based upon their speed in traveling in the nervous system (fast and slow pain), the length of time the pain has continued (acute or chronic pain), or the anatomical etiology of the sensations (somatic or visceral pain). This article discusses the anatomy and physiology of pain sensations, concentrating on acute pain mechanisms. Limited discussion is offered regarding the modulation of pain sensations, and there is a brief overview of visceral pain. Discussion of chronic pain pathophysiology is included in the article by Hansen on chronic pain elsewhere in this issue.
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